Advertisements

Posts Tagged ‘ Medical research ’

Good news for prostate cancer patients…especially for those not responding to present day treatments…research has uncovered another potential drug that can be useful in breathing new life in the battle against cancer. With every ground-breaking news …comes hope of a another day to see the sun-rise…keep fighting and never surrender…

A new drug that tackles advanced prostate cancer in three different ways has passed its first hurdle towards being approved.

Scientists reported promising early trial results using galeterone, which is designed to treat cancer that no longer responds to hormone therapy. However, researchers counselled caution as tests on the “triple whammy” drug have been carried out on only a small number of patients.

In their tests, scientists based at Harvard University reported that galeterone reduced levels of prostate specific antigen (PSA), a prostate cancer blood marker, by 30% or more in about half of patients. Eleven patients had PSA reductions of 50% or more, and in some there was significant shrinkage in tumour size.

A total of 49 patients took part in the phase one study, which primarily looked at safety and dosing levels. All had “refractory” or “castration resistant” cancer that had ceased to respond to hormone therapy. Currently there is little doctors can do to help prostate cancer patients who progress to this stage.

Galeterone works in three ways: by blocking “receptor” proteins that respond to testosterone; by reducing the number of receptors in tumours; and by targeting an enzyme that is linked to hormone pathways involved in the cancer. Trial leader Dr Mary-Ellen Taplin described the galeterone study as “exciting for those of us in the medical community treating this life-threatening cancer”.

The findings were presented at the annual meeting of the American Association for Cancer Research in Chicago. A larger phase two trial, focusing on the drug’s effectiveness, is planned later this year.

The results were welcomed by Dr Kate Holmes, head of research at the Prostate Cancer Charity. “This very early stage research, conducted among a small group of men, indicates that galeterone shows potential as a new treatment for men with advanced prostate cancer.

“This new drug is in its infancy and full results have yet to be published, meaning that it is simply too soon to tell whether or not this drug is capable of living up to its early promise.

“Men in the final stages of prostate cancer have very few options available to them and we desperately need to increase the number of effective treatments,” she said.

“The researchers have plans to test the drug in a further trial, to fully investigate the full side-effects and safety of treatment. We look forward to reading the full publication of this study in due course, and await with anticipation the results of further trials.”

There’s has always been discussion on the pros and cons of vitamin supplementation in our diets. I see no harm in taking vitamin D and other supplements as long one stays within the normal dosage recommedated by physicians and FDA guidelines. Usually common sense dictates following the instructions listed on the bottle or physician’s orders. Never decide to begin ingesting supplements until your have discussed doing so with your family doctor first. Vitamin D is an important vitamin from strong bones,growth, and for many chemical reactions that occur within our bodies. Moderation is the key to absorbing sufficient Vitamin D. As for sunshine….be careful not be burn ..wear sunscreen protection…

Vitamin D is in the news again, and while the experts squabble over it, I’m off to buy myself some supplements. The chief medical officer for England has told GPs like me to advise those at risk to take supplements. And since half the adult population of the UK is lacking vitamin D in the winter months and deficiency is being linked to a growing list of health problems, I can’t see a good reason not to take a small multivitamin a day – at least until the sun comes out. I’ll stick to the recommended daily amount as you can have too much of a good thing, even vitamins.

Vitamin D is essential for bone growth and health, and deficiency can cause rickets in the young and a condition called chondromalacia in adults. You wouldn’t think rickets still existed in the UK but it probably never went away and is increasingly recognised as a cause of fractures in susceptible children.

Recently two parents, Rohan Wray and Chana al-Alas, were accused of murdering their four-month-old baby who died two years ago from sudden infant death syndrome (Sids, also known as cot death). The baby, Jayden, was found to have multiple injuries and the parents were accused of shaking the baby to death. But pathologist Dr Irene Scheimberg, based at Royal London Hospital, found evidence of rickets in Jayden at postmortem and the judge directed the jury to acquit.

Since that tragic case, Scheimberg says she has discovered vitamin D deficiency in eight further cases of Sids and in 30 cases of children who have died of various causes and had postmortems. A colleague of hers, Dr Marta Cohen, working in Yorkshire has also found vitamin D deficiency in 18 out of 24 cases of Sids and in 45 babies under the age of one, who died of other causes. Both doctors are calling for further investigation into the implications of vitamin D deficiency and highlighting the need to be aware of rickets in cases of Sids, which can be mistaken for non-accidental injury.

This adds weight to those calling for widespread vitamin D supplementation in the UK. Advice from the chief medical officer for England, Sally Davies, was for at-risk groups – which includes pregnant and breastfeeding women, children aged six months to five years old, people aged 65 or over, people who are not exposed to much sun (the housebound, those who cover up their skin for cultural reasons and people who have darker skin, whose bodies are unable to produce vitamin D as easily) – to take vitamin D. But there have been calls to introduce supplements for all the population in Scotland, because of high levels of multiple sclerosis which may be linked to vitamin D deficiency. Ryan McLaughlin, 13, launched a campaign, Shine on Scotland, in response to his mother’s diagnosis of MS, while Professor George Ebers of the Nuffield department of clinical neurosciences at Oxford University believes the evidence is now good enough to justify dosing the entire population with vitamin D. Professor George Ebers of the Nuffield Department of Clinical Neurosciences at Oxford University is quoted, saying that he believes the evidence is now good enough to justify dosing the entire population with vitamin D. Last month, his team published evidence of a link between MS and an inherited tendency that leads to vitamin D deficiency.

Scotland’s chief medical officer, however, Sir Harry Burns, says in the same article he thinks there needs to be “broader scientific consensus” before change is considered. He warns that dietary supplements can cause harm and that we need to wait for good randomised studies in large populations. He wants to wait for the conclusions of a review of the evidence by the UK government’s scientific advisory committee on nutrition in 2014.

But Ebers says that is too long. He reflects that there was evidence to support recommending folic acid supplementation for all pregnant women to prevent problems like spina bifida, many years before the public health authorities backed it.

Bruce Hollis, professor of paediatrics and biochemistry at the Medical University of South Carolina, agrees, insisting there’s no point waiting for a large randomised trial because it’s unlikely to ever happen. He says it would be hard to attract funding for an expensive, large scale trial as drug companies would be unlikely to make a profit on cheap vitamin supplements.

The best source of vitamin D is sunlight on the skin. Vitamin D is also found in a small number of foods (oily fish, eggs, cheese and meat) but it is difficult to get enough vitamin D from diet alone. In the UK, all margarines and infant formula milks are already fortified with vitamin D and it is also added, in small amounts, to other foods such as breakfast cereals, soya and some dairy products,. Breastfeeding mothers need adequate vitamin D levels of their own to ensure their babies get enough.

You can buy single vitamin D supplements at most pharmacies and supermarkets. Pregnant women who take vitamin D as part of a multivitamin should avoid supplements containing vitamin A (retinol), which can be harmful in pregnancy.

While the experts continue to debate, we may all be well advised to take a daily vitamin D supplement and expose our skin to whatever weak winter sunshine we can.

It’s more often than not that mortality figures are under-estimated or lower than reported…are you really surprise? Malaria is a serious disease… No matter how strong you may think you are…your immunity to malaria may not be enough to succumb to the disease. How long will the insecticides to effective in keeping the populations of mosquitoes at bay?….well until they develop a resistance to the chemicals we are using…..there’s got to be a more natural approach in curbing the over-population of these blood sucking critters..! Any ideas out there…share it with us…

Decades of assumptions about the lethality of malaria have been overturned by the publication of a paper in the Lancet from an academic institute in Seattle which says the disease kills twice as many as everybody thought. Even more extraordinary – it would seem that conventional wisdom about the disease has been wrong all this time.

It does not just kill babies and children under five — it kills adults too, in nearly as large proportions.

The Institute of Health Metrics and Evaluation has astounded the global health community by claiming it has been fighting malaria apparently with one hand behind its back. The death toll has come down since 2004, thanks to huge efforts to get insecticide-impregnated bednets to households and treat those who are sick with better drugs, but all the while an older age group has been neglected.

“These are certainly results which surprised us when we first did the analysis,” said Steve Lim, one of the authors of the Lancet paper. “It is new to what is taught in public health and medical school, which is that when kids are exposed to malaria at a very young age, it conveys immunity.”

Only last year the World Malaria Report gave mortality figures which are half those the institute has found – 655,000 deaths compared to 1.2 million. It is an extraordinary gulf and there will be lots of debate about the statistical methods used by the Seattle team.

But the institute has form. This is part of a five-year project, funded by the Bill and Melinda Gates Foundation, to obtain the best possible data for the toll of death and disease from vario

As technology races ever so quickly into the future, it does so by making daily activities in the laboratory much more easier to perform tests. It’s amazing how much information can be retrieved from just one drop of human blood. The benefits of such tests being done more quickly and inexpensive is that we can now do them more frequently. By adopting a more active role in our health and performing frequent blood tests , we can detect an underlaying disease before it progresses too far…and perhaps save our own lives..

When a doctor wants to carry out a test, she will probably prick you with a needle, fill up several test tubes of your blood, label, package and send them to some centralised hospital laboratory. Technicians will then take the contents, perform the various biochemical analyses needed, write up the results and send back the documentation in a few weeks, perhaps longer if there’s a backlog.

The process is slow and labour-intensive. What if you could reduce the whole business to a few minutes? What if, for the majority of ailments or questions, the doctor only needed a drop of your blood and could test you for viruses or cancers while you wait in her surgery? With a lab-on-a-chip, that is already possible.

Quick tests are not a new idea – pregnancy tests can be done at home and diabetics can quickly and easily measure their blood sugar levels using only a drop of blood – but complex diagnoses still need labs and technicians.

“With a lab-on-a-chip you can do a quick diagnostic test and get information right there, which is very useful when somebody’s got a disease that’s got a very short timeline to be treated,” says Mark Morrison, CEO of the Institute of Nanotechnology in Stirling, UK. “What it effectively does is miniaturises and compacts all the different processes that a researcher or a technician in the diagnostic lab uses.”

The lab-on-a-chip shrinks the pipettes, beakers and test tubes of a modern chemistry lab onto a microchip-sized wafer of glass or plastic. Perhaps you want to know which viruses are in a sample of blood? Or, on the battlefield, which biological warfare agent is present in a soldier’s bloodstream? Put in a drop of blood at one end and the carefully carved channels take its constituent molecules past a circuit of nanometre-sized chemical and physical tests that poke, prod and characterise them to answer your question, however complicated. A chip developed by the University of Alberta, for example, can screen for chromosome mutations that cause a range of cancers.

The platform blurs nanotechnology, biotechnology and micro-electronics. And it is not specific to medicine – it is being developed for environmental monitoring of pollutants and, increasingly, in basic scientific research to speed up the once-tedious aspects of examining genes or testing the properties of new materials.

Prof Tom Duke at the London Centre for Nantechnology has been working on a chip that can detect whether a blood sample contains HIV. Current tests require testing in large laboratories staffed by skilled clinicians, which is a hindrance if you want to test people in resource-poor countries where the disease is rife.

Duke’s chip simplifies that process using a sensor that only requires a drop of blood at one end. The blood is separated into its parts by an array of nanometre-sized silicon pillars in the sensor and the biggest bits – such as blood cells and large proteins – are trapped. Any virus particles pass between the pilars to the other end of the sensor, where they are attracted to a series of tiny cantilevers coated with antibodies. These are, in essence, mini diving boards that bend when something lands on them, and that deflection can be measured by bouncing a laser off them. The more the diving boards are deflected, the more virus is present. “This platform can be used for pretty much any viral or bacterial disease,” says Duke.

There are several advantages to the lab-on-a-chip approach, beyond the convenience of being able to test in the field. The test sample required is much smaller because of the sensitivity of the chip, which is useful if you need to measure trace gases in the atmosphere or the very earliest stages of a disease when the chemical markers in the blood are low in number and would probably be missed by standard tests.

“Potentially you can detect the presence of, for example, cancer or diabetes at a much earlier stage and then treat it more effectively,” says Morrison. “If you treat the disease earlier on, you have a much greater chance of success.”

The Simbas chip, designed by a team of researchers led by Ivan Dimov at the University of California, Berkeley, can detect a biological component in blood at a concentration of around 1 part per 40 billion. “That can be roughly thought of as finding a fine grain of sand in a 1,700-gallon sand pile,” says Dimov. The self-contained chip can get results from a drop of blood in 10 minutes, without the need for any external pumps, tubes or power supply.

Researchers interested in basic physiology are also finding a use for these sophisticated mini laboratories. Scientists at Harvard University have created a lung on a chip that contains several types of tissue and can be used in experiments to understand basic function. They can simulate flowing blood, introduce pollutants and toxins to see how the “lung” reacts and even stretch and contract the cells to simulate breathing.

The technology will no doubt get faster, cheaper and more abundant. But there are some ethical questions coming along the pipeline, along with the technical ones. Most important, while it is still in its infancy and still relatively expensive, who gets access to it? And, since many of the devices will be used to test for an individual’s susceptibility to specific genetic diseases, another question is who should be able to access to that information? “As a scientist I’d say screen everybody for every disease because then you know who is going to get something and you can treat them early on,” says Morrison. “But that’s maybe looking at it from a utopian point of view.”

The dystopian alternative is a precautionary note rather than an inevitability and, in any case, debates around future access to genetic and medical data are already under way, thanks to a rapidly improving arsenal of medical and environmental sensors. Miniature laboratories on silicon and glass chips are another, invaluable tool in that arsenal.

The Guardian is working in association with the European Union’s NanoChannels project to create a portal for information on the technical and ethical challenges associated with nanotechnology

Resveratol has been known for some time to be of benefits to a healthy life-style. Recent studies have uncovered additional qualities that may encourage more persons to add resveratrol to their diets. Reducing blood sugar is a wonderful metabolic side effect that can benefit the millions of people diagnosed with diabetes. So perhaps resveratrol deserves a closer look at…..

Taking supplements of a substance found in grape skin can lower sugar and fat levels in the blood and reduce blood pressure, according to a small study.

Scientists who gave tablets containing purified resveratrol to obese men found it had some metabolic effects similar to those from exercise and calorie restriction, including lowering blood pressure and blood sugar levels.

Research in animals over the past decade has suggested the compound can slow the development of age-related diseases and increase lifespan. However, these studies have attracted growing criticism and have yet to be replicated in humans.

“The effects of resveratrol were modest but they consistently point towards beneficial metabolic adaptions,” said Prof Patrick Schrauwen of Maastricht University in the Netherlands, who led the new study. Although the chemical is found naturally in grape skin and red wine, there is no suggestion that it would be possible to ingest enough of it from these sources to gain the beneficial effect.

Prof Schrauwen and colleagues gave 11 obese men either a daily 150mg resveratrol supplement or a placebo for 30 days. Four weeks later, the two groups swapped over so that those who took the supplements first time around were given placebos and vice versa.

Regular measurements showed resveratrol lowered blood sugar levels and improved insulin sensitivity, as well as cutting triglycerides – fats found in the blood that can increase heart disease risk. Resveratrol also reduced both sleeping and resting metabolic rate and cut blood pressure.

Previous research has shown that calorie restriction can extend lifespan in laboratory animals. Some studies suggest it also offers protection from diseases such as cardiovascular disease and type 2 diabetes, though this remains controversial.

Calorie restriction works in a similar way to resveratrol, by triggering the production of a protein called SIRT1 which improves metabolic function and keeps cells healthy in the face of stress.

Muscle biopsies carried out by Prof Schrauwen’s team confirmed that participants taking resveratrol saw increased SIRT1 levels. They also strongly suggested the beneficial effects on metabolism were associated with improved functioning of mitochondria, the energy factories within cells.

“Healthy people are good at switching efficiently from using fat as an energy source to glucose in the blood when it becomes available,” said Prof Schrauwen. “The results of our pilot study tended to suggest that might be part of the link to the beneficial health effects of resveratrol, but that needs further study.”

Prof Schrauwen, acknowledging that his sample size was small, said he was seeking funding for a larger and longer trial. “This is small, proof of principle study, but the results are so promising that I think it is important that we conduct a bigger study,” he said.

Taking aspirin seems to be getting more popular these days…that is good news for the pharmaceutical companies..but can also be good news for the rest of us…perhaps taking aspirin is not only good to take to lower the risk of an heart attack by thinning out the blood, but it may help us lower the risk of developing some types of cancers…only time will tell if this idea has any merit.. consult your physician before taking or adding any medication to your diet.

Some people with a family history of cancer could halve their risk of developing the disease by taking daily doses of aspirin, according to the results of a 10-year trial of the treatment.

The study shows that regularly taking the medicine cuts the risk of bowel cancer by more than 60% in those with a particular genetic predisposition to get the disease – as well as reducing the risk of other hereditary cancers.

Scientists who led the study said people with several family members with cancers other than breast, blood and prostate might be advised to start taking aspirin daily from the age of 45.

They said those without a family history of the disease might also consider doing so, but that they should make a personal assessment of the risks and benefits and get medical advice. Anyone thinking of taking the drug regularly should consult their doctor first.

Doctors already prescribe low, daily doses of aspirin to people at increased risk of heart attacks and strokes, and evidence has been growing of anti-cancer properties for 20 years. However, this is the first long-term, randomised controlled trial to show such an effect.

The trial involved people with Lynch syndrome, a genetic abnormality that predisposes carriers to develop bowel cancer and other solid organ cancers including endometrial, ovarian, stomach, kidney, oesophageal, brain and skin tumours.

The condition affects at least one in 1,000 people. Carriers are around 10 times as likely to develop cancer and often do so at a young age.

Professor John Burn of Newcastle University, who led the study, estimated that if all 30,000 or so people with Lynch syndrome in the UK were to start taking two aspirin tablets a day then some 10,000 cancers would be prevented over the next 30 years, saving about a thousand lives. The downside of the treatment is that around an extra thousand people would develop stomach ulcers as a side-effect.

“People with a genetic susceptibility are a model system,” said Burn, whose work is published on Friday in the Lancet online. “They are more sensitive to the environmental triggers to cancer.

“If we can do something to change cancer progression in people at high genetic risk, then that’s telling us what we might all benefit. But we are not making a recommendation for the general population. Everyone can take this evidence and make their own choice.

“In between you have the people who have a family history [of cancer]. Those individuals may well decide to put themselves on aspirin and that would be a reasonable conclusion from the data currently available.”

Between 1999 and 2005, about half of a group of 861 Lynch syndrome carriers were given two aspirins (600mg) a day, while the rest took placebos.

By 2010 those who had taken aspirin for at least two years were 63% less likely to have developed bowel cancer.

Looking at all forms of the disease, almost 30% of those in the placebo group developed a Lynch syndrome-related cancer, compared with 15% for those given aspirin.

The most common side effects associated with taking aspirin are gastrointestinal ulcers and stomach bleeding. There is also an very small increased risk of haemorrhagic stroke, in which a blood vessel in the brain bursts.

There was no difference in the proportions of the study groups suffering such side-effects.

Burn added that he takes low-dose aspirin tablets as a preventative measure. “That was a balanced judgment based on weighing risks and benefits. I know I might get an ulcer or a cerebral bleed but I’d rather not have a heart attack, stroke or cancer. That’s my choice.”

Aspirin is a synthetic version of the active component of willow bark, salicylic acid, which has been used as a medicine for its anti-inflammatory properties for hundreds of years. Salicylates also trigger programmed cell death to help diseased plants contain the spread of infection.

“It’s not a huge stretch to think that if salicylate induces programmed cell death in plants to kill infected cells, maybe it’s doing similar things in the animal kingdom to enhance the death of aberrant cells causing cancer,” said Prof Burn.

“This adds to the growing body of evidence showing the importance of aspirin, and aspirin-like drugs, in the fight against cancer and emphasises how critical it is to carry out long-term international research,” said Prof Chris Paraskeva, a bowel cancer expert at the University of Bristol.

Telomere Science still has a lot of work ahead of itself…there are many factors that contribute to the aging process…so if a test can predict when I will die…perhaps in the future we can manipulate the strands of our DNA to extend our lives to 120 years of age. It sounds like science fiction ….but remember many ideas have started out as an impossibility…only to develop into a feasible application to enhance the quality of life.

As a taxi takes me across Madrid to the laboratories of Spain’s National Cancer Research Centre, I am fretting about the future. I am one of the first people in the world to provide a blood sample for a new test, which has been variously described as a predictor of how long I will live, a waste of time or a handy indicator of how well (or badly) my body is ageing. Today I get the results.

Some newspapers, to the dismay of the scientists involved, have gleefully announced that the test – which measures the telomeres (the protective caps) on the ends of my chromosomes – can predict when I will die. Am I about to find out that, at least statistically, my days are numbered? And, if so, might new telomere research suggesting we can turn back the hands of the body’s clock and make ourselves “biologically younger” come to my rescue?

The test is based on the idea that biological ageing grinds at your telomeres. And, although time ticks by uniformly, our bodies age at different rates. Genes, environment and our own personal habits all play a part in that process. A peek at your telomeres is an indicator of how you are doing. Essentially, they tell you whether you have become biologically younger or older than other people born at around the same time.

The key measure, explains María Blasco, a 45-year-old molecular biologist, head of Spain’s cancer research centre and one of the world’s leading telomere researchers, is the number of short telomeres. Blasco, who is also one of the co-founders of the Life Length company which is offering the tests, says that short telomeres do not just provide evidence of ageing. They also cause it. Often compared to the plastic caps on a shoelace, there is a critical level at which the fraying becomes irreversible and triggers cell death. “Short telomeres are causal of disease because when they are below a [certain] length they are damaging for the cells. The stem cells of our tissues do not regenerate and then we have ageing of the tissues,” she explains. That, in a cellular nutshell, is how ageing works. Eventually, so many of our telomeres are short that some key part of our body may stop working.

The research is still in its early days but extreme stress, for example, has been linked to telomere shortening. I think back to a recent working day that took in three countries, three news stories, two international flights, a public lecture and very little sleep. Reasonable behaviour, perhaps, for someone in their 30s – but I am closer to my 50s. Do days like that shorten my expected, or real, life-span?

People with similar worries – or, perhaps, just Woody Allen-style neuroses about their health – have begun to contact the company set up by Blasco. Requests have poured in from around the world since a headline writer at the Independent, perhaps misled by Life Length‘s ambiguous name, invited readers to find out about “The £400 test that tells you how long you’ll live.” The internet did the rest.

Originally set up to help researchers and the pharmaceutical, health food and cosmetics industries test the impact of their products on telomeres, the flood of individual requests has caught Blasco’s still tiny company by surprise. But the test is available, as of this month, via doctors in Spain and Portugal and there are plans to make it easier to carry out in the UK and the US as soon as possible. It sees a potential gold-mine in testing of what it calls people’s “biological age” – though it is by no means alone in the field. So what can Blasco tell me about my test?

“You actually have very good news,” she says, pointing at a chart that looks as if it has been blasted by shotgun pellets. My telomeres – especially the more dangerous, shortest ones – are in better shape than would be normal for my age. The pellet points are individual results from those people who have been tested and introduced into this database so far, and the red dot representing my blood sample is on the better side of the two graphs Blasco shows me. One graph shows median telomere length, while the other shows how many crucially short telomere endings I have. In each case, a line on the graph shows the average result against age. The test on some 100,000 of my telomeres, compared with the other results on the admittedly small database being used by Life Length when this test was done in the summer, give me a “biological age” six years below my real age. With only 90 other men on the chart so far, all with different lifestyles and genetic backgrounds to mine, I should avoid feeling smug. Eventually, when there are thousands or more on the database, I might get a better idea of what results people more like me should expect. I have a reasonably healthy lifestyle, after all, and previous generations on both sides of my family have been long-lived.

Blasco, obviously, disagrees. So does Elizabeth Blackburn, who shared the Nobel prize for telomere research with Greider and Jack Szostak, and has set up her own Telome Health company to start offering tests later this year.

Blasco compares the current state of telomere testing to the early days of cholesterol tests – and believes it should become common once the price drops and research is done to beef up databases, improve interpretation and create telomere-restoring treatments. “This is a different kind of marker. It is a new, molecular marker. Even though we measure telomere length in blood cells, it has been shown to be an indicator of the degree of telomere shortening in the whole organism,” she says. “And we think it is very powerful, based on what we know from hard science.” Even so, she is insistent that the test is not a magic measure of individual life length. “We don’t tell anyone how long they will live.

“It is the doctor – and we want to do this with doctors – who will tell you what is known about the meaning of this measurement and what you can do and what you cannot do,” says Blasco. In fact, the benefits of telomere science still lie mostly in the future. As with early cholesterol tests, a doctor is currently unable to tell you much about what those results mean – or what you can do about a bad result, beyond fairly obvious advice about looking after your health.

I notice that a few of the 90 men on my chart have apparently alarming results. Their telomeres indicate a “biological age” 20 years or more higher than their real age. This means that, at least statistically, they may be much closer to death than most people their age. One of these men comes from a family with a long history of early cancers, according to Life Length’s CEO Stephen Matlin. He has offered those with worryingly high results a free second test after three months, to see whether anything has changed. My report also warns, however, that results may reflect temporary illness or ongoing medical treatments – effectively skewing them. And some results on the chart look plain bizarre. One tester, for example, appears to have – at least statistically – a biological age of around 120. Two people aged above 60, together with a clutch of 30-year-olds, have an estimated biological age below zero – presumably because their telomeres are in better shape than might be expected of the average baby. Life Length said this reflected the fact that little research had been done on the telomeres of the very young.

Individual testing, then, is still in nappies. Far more exciting are the possible future advances to come from telomere research, says Blasco. “One is telomerase activation, because of its potential to reverse ageing. And proving which diseases can benefit from telomerase activation, in order for this to be something druggable.”

“Some of the new [research] papers appearing in top journals are to do with telomorase activation,” she says. “That is one aspect. The other is that we are seeing a lot of epidemiological studies showing correlations between telomere length and certain diseases, and which habits are good or bad for telomere length.”

She says the idea that telomeres can be “re-elongated” and, hence, that biological age can be reversed does not open the door to immortality – even if scientists have been able to extend a mouse’s age by up to 40%. “That’s a lot, but nobody has been able to make a mouse that is immortal,” she says.

It does, however, throw up philosophical and ethical dilemmas. The US Food and Drug Administration (FDA), for example, refuses to approve drugs that are simply designed to prevent ageing. “Although I – and many more scientists – believe ageing is the cause of diseases, this is not perceived like that yet by the FDA,” says Blasco. “But what is clear is that there are a number of diseases associated with ageing which are caused because our cells age.”

Activating telomerase to counter that, she says, might help prevent major illnesses and allow drugs to be approved by the FDA. If drugs are found to activate telomerase and prevent, say, Parkinson’s disease, Alzheimer’s disease or some cardiovascular problems then the inevitable result will be not just a healthier life, but also a longer one.

Blackburn agrees that the idea that the new tests can tell you your life length is silly, but she insists that the evidence connecting telomere length and disease risk is becoming clearer.

“We and other groups are seeing clear statistical links between telomere shortness and risk for a variety of diseases that are becoming very common, such as cardiovascular disease, diabetes and certain cancers,” she told the nature.com website in August. “We have also looked at chronic psychological stress, including depression and post-traumatic stress disorder, and more and more we see associations with telomere shortness. There are even links with education — in one study telomere shortness was related to not finishing school. We’re seeing the data unfolding in front of us. A lot of them are not published yet.”

So what has telomere testing done for me? Not a lot, frankly, though I might have reacted differently had I been dangerously off the chart. Nor am I a woman in her 30s, who might like to know how fast the biological clock that may eventually limit fertility is ticking.

I am tempted to repeat the test again, mainly out of a competitive desire to get better, but only if (as on this occasion, when Life Length waived the $500 fee) I can get it for free. Far more interesting, however, has been the glimpse of the future – when telomere testing, and popping pills to repair the tips of our chromosomes, may allow us to live both longer and healthier. I am persuaded, too, that the aim should be to make sure we live our years out in good health. So why all the rushing about? Time, perhaps, to take things more calmly.

Progress is being made in cancer research…side effects experienced by patients during chemotherapy can be reduced or even eliminated in the near future…a better delivery system of introducing anti-cancer therapy can also leave healthy cells intact…the “smart bomb” is here…

Cancer researchers have developed a “smart bomb” treatment that can target tumours with drugs while leaving healthy body cells intact. The technique means that patients will suffer fewer side-effects from the toxic drugs used in chemotherapy.

The side-effects of cancer therapy – including hair loss, nausea and suppression of the immune system – can be debilitating. In many cases, the effects of the drugs can contribute to the ultimate cause of death.

In experiments on mice, Laurence Patterson of the University of Bradford found that he could localise a cancer drug to the site of tumours and thereby limit its toxic impact in the body. All the animals, which had been implanted with human cancer cells responded to the targeted treatment and saw their tumours shrink. In half the animals, the tumours disappeared altogether. Professor Patterson will present his work at the British Science Festival in Bradford on Monday.

“We’ve got a sort of smart bomb that will only be active in the tumour and will not cause damage to normal tissue,” he said. “It’s a new cancer treatment that could be effective against pretty much all types of tumour – we’ve looked at colon, prostate, breast, lung and sarcoma so far, and all have responded very well to this treatment.”

The drug is based on a modified version of an existing cancer drug called coltrazine. In normal situations, this drug is delivered as part of a patient’s chemotherapy regime and, in addition to attacking cancer cells, it can kill healthy cells, too. “There are many agents currently used in the clinic for the treatment of cancer that are essentially poisons,” said Patterson.

“Normal chemotherapy can often be the cause of death of the patient as opposed to dying from the tumour growth itself. Any treatment that is a poison that can be retained and is only active in the tumour is clearly very attractive.” Patterson’s team has designed a way to make the coltrazine active only when it comes into contact with a tumour. They did this by attaching a string of specific amino acids to the coltrazine, which made the drug inert. In this state, it can wander through the body freely and will not kill any cells it comes into contact with. But when the drug reaches the site of a solid tumour, the chain of amino acids is removed by an enzyme present on the surface of the cancer, called MMP-1. At this point, the coltrazine becomes active and can do its work in killing nearby cells.

MMP1 is used by tumours to break down the cellular environment around itself and to enable the tumour to dig a path through normal tissue. It also gives the tumour access to nutrients and oxygen by encouraging the normal blood supply of a person to grow towards it. “If you can starve that tumour of that blood supply, then you shut off its ability to grow and move around the body,” said Patterson.

In the experiments, he said, all the mice responded to the treatment. “Sometimes, the treatment is so effective, you remove the ability of that tumour to grow – you appear to cure the mouse. In some studies, we were able to cure half the mice: these animals no longer had any tumour growing in them and they appeared healthy for the 60 or so days of the trial.”

An important use of the technique is that it can reach tumours that have spread throughout the body.

Paul Workman, head of cancer therapeutics at the Institute of Cancer Research, said: “This is an interesting new approach to targeting tumour blood vessels that solid cancers need for their growth. The project is still at quite an early stage, but the results so far look promising in the laboratory models that have been studied. If confirmed in more extensive laboratory studies, drugs based on this approach could be very useful as part of combination treatments for various cancers.”

The Bradford scientists hope that, with adequate funding, their drug delivery system could enter phase 1 clinical trials on people within 18 months.

Research advancements into the understanding of the Ebola virus and eventually a cure will no doubt lead way to other many discoveries. Science is at the verge of a flood of discoveries that will change the destiny of medicine forever.

One of the world’s most feared pathogens, the Ebola virus, has a key structural weakness that could be vital in developing drugs to treat the fevers it triggers, US researchers announced in Nature last week. The group say they have bred mice that produce low levels of a protein known as Niemann-Pick C1 which transports cholesterol inside cells. The mice then survived exposure to Ebola, which causes a haemorrhagic fever, and to a cousin pathogen, the Marburg virus.

“This research identifies a critical cellular protein that the Ebola virus needs to cause infection and disease,” said one of the lead scientists in the project, Sean Whelan of Harvard Medical School. “It also improves chances that drugs can be developed that directly combat Ebola infections,” he said.

Ebola fever was first detected by doctors in the 1970s in villages along the Ebola river in the Democratic Republic of Congo and is usually fatal in humans. There have been at least two dozen Ebola outbreaks in Africa though doctors still do not know exactly how the virus is spread. There are no vaccines or drugs to fight it.

The virus is known to interfere with the cells that line the interior surfaces of blood vessels and with the process of blood coagulation. As a result, it causes blood vessel walls to become damaged and to rupture.

The new research announced at Harvard is therefore extremely important. It indicates that the protein Niemann-Pick is used by the Ebola virus to get deep inside cells. “This virus needs this protein,” said Kartik Chandran, of Albert Einstein College of Medicine in New York. “Mice that have less of this protein are very resistant to being killed by Ebola and the Marburg virus.”

Crucially, Chandran has also been involved in work that led to the discovery, in 2005, of a compound that has demonstrated considerable promise in being able to block the Niemann-Pick protein in human cells, according to a separate paper that was published in Nature last week. “Essentially, this compound can block infection by the virus,” said Chandran.

The compound has not yet been tested in mice, and would still need to show it is effective in non-human primates. Chandran said blocking Niemann-Pick in the long term would probably cause illness.

The researchers involved in the studies say they are very optimistic that the new understanding they have built up about the behaviour of the Ebola virus and the means by which it gets into cells may eventually lead to treatments. However, they acknowledge it will take many years, and possibly even a decade of further research and studies, before treatments would be available for human use.

There’s a pill for every ailment that exists but we need to be careful not to take a combination of medications that could prove to be lethal. All too often an individual may have 2 or 3 doctors that may be prescribing a regiment of medications..we need to stop taking so much medicine…unfortunately these doctors are not consulting with each other. Patients are also not informing their doctors of all medications being prescribed. Tell your physician about all medications you are talking…and if possible ..eliminate those that are not needed..

The combined side-effects of commonly-used drugs can increase the risk of death and brain impairment in people over 65, according to a study of more than 13,000 people. Researchers have urged people who are taking a combination of medicines to review their intake with their doctors in light of the findings.

The study was part of the Medical Research Council’s Cognitive Function and Ageing Studies project and looked at a specific class of commonly used drugs being taken by people over 65 over a two-year period.

The list includes over-the-counter medicines such as Piriton and Nytol, and the anti-depressant paroxetine, used in Seroxat.

Fox rated the activity of different drugs on a messenger chemical in the brain on a three-point scale, with 0 for no effect and 3 for a severe effect. The results, published in the Journal of the American Geriatrics Society, showed that around 20% of those people who took a regimen of drugs that scored more than 4 on the scale had died in the two years of the study, compared with only 7% of those not taking any medication in the drug class. “For every extra point scored, the odds of dying increased by 26%,” said Fox. “We found it was a cumulative risk – not just the severity of the blockade but the number of drugs as well.”

Ian Maidment, a pharmacist at Kent and Medway NHS & Social Care Partnership Trust, said that many doctors, nurses and pharmacists may not be aware that these medicines have these problems and cited overuse of drugs as one of the factors adding to the cumulative burden on people over 65. “Often you see anti-histamines, which have a high burden, for hay fever and they are continued in the depths of winter when there is snow on the ground. The problem is that someone with dementia can’t say, ‘I don’t need anti-histamine,’ so it’s continued when it’s not needed.”

Participants in the study who were taking drugs with a combined score of more than 5 also showed cognitive decline – they scored more than 4% lower in cognitive function tests compared with those who were taking no anticholinergic drugs.

“The message here is for doctors to regularly review the medication of your older patients,” said Susanne Sorensen, head of research at the Alzheimer’s Society. “The message to patients is to ask, when you’re given medication, the pharmacist if what you’re buying at the counter has any side-effects and may be bad in combination with the other drugs you take..”

Professor David Nutt, president of the British Neuroscience Association and vice-president of the European Brain Council, said that the negative effects of this class of drugs on brain and cardiac function had been known for decades and the latest study reinforced the dangers.

Dr Tim Chico, an honorary consultant cardiologist at the University of Sheffield, added that all drugs had possible side effects, but the new results should not lead anyone to stop current medications without discussing this with their doctor first. “Before starting any drug, it is important for the doctor and patient to discuss the possible benefits of the treatment, compared with the potential downsides, so that the patient can make an informed decision. As a cardiologist, many of the drugs I use (such as beta-blockers) have been definitely proven to make people with heart disease live longer, so it’s important to balance these proven benefits against the risk of side effects.”

A discovery of the master switch gene(KLF14) linking diabetes and obesity related diseases has been found by scientists (go to Yahoo.com for more information)…wow I say that is great news….perhaps this can give us a clearer picture and perhaps a cure for metabolic diseases in the future…keep you fingers crossed….below is an article linking dementia and diabetes…

People who are obese in middle age are at almost four times greater risk of developing dementias such as Alzheimer’s disease in later life than people of normal weight, according to a study released today.

The study, published in the journal Neurology, examined data on more than 8,500 people over the age of 65. Of the sample, 350 had been diagnosed with Alzheimer’s disease or vascular dementia and a further 114 had possible dementia.

Scientists used records of the participants’ height and weight in the decades before and found that those who had been overweight in middle age had a 1.8 times (80%) higher risk of being diagnosed with dementia in later life. But for obese people, classified as those having a body mass index (BMI) of 30 or above, the risk soared. People with midlife obesity had an almost four times (300%) higher risk of dementia.

“Currently, 1.6 billion adults are overweight or obese worldwide and over 50% of adults in the US and Europe fit into this category,” said Weili Xu of the Karolinska Institutet in Stockholm, who led the research. “Our results contribute to the growing evidence that controlling body weight or losing weight in middle age could reduce your risk of dementia.”

According to the Alzheimer’s Society, around 750,000 people in the UK suffer from dementia, more than half of those with Alzheimer’s. By 2021, a million people will be living with dementia.

Obese people are classified as those with BMI greater than 30, overweight people are those with a BMI between 25 and 30. Between 20 and 25 is classified as normal. Almost 30% of those in the study, 2,541 in total, had been either overweight or obese between 40 and 60 years of age.

“Although the effect of midlife overweight on dementia is not as substantial as that of obesity, its impact on public health and clinical practice is significant due to the high prevalence of overweight adults worldwide,” said Xu.

Susanne Sorensen, head of research at the Alzheimer’s Society, said: “This robust study adds to the large body of evidence suggesting that if you pile on the pounds in middle age, your chances of developing dementia are also increased.By eating healthily and exercising regularly, you can lessen your risk of developing dementia. Not smoking and getting your cholesterol and blood pressure checked regularly is also very important.”

Xu agreed that healthy living in middle age can help to reduce a person’s risk of developing dementia in later life and added that a person’s experience of education also played a role in the rate of decline of the brain. “Based on this data, every one year in higher education is associated with about 10% reduced risk of overweight and obesity, and 8% decreased risk of dementia.”

Exactly how excess weight can influence the degradation of the brain is not certain, but Xu said there could many possible mechanisms. “Higher body fat is associated with diabetes and vascular diseases, which are related to dementia risk,” she said.

In addition, fatty tissue is the largest hormone-producing organ in the body and it can produce inflammatory molecules which may affect cognitive functioning or the process of neurodegeneration.

Sorensen said that further research was needed to find the links between being overweight and dementia. “One in three people over 65 will die with dementia, yet research into the condition is desperately underfunded.”

The Alzheimer’s Society has launched the Drug Discovery programme, which it says could lead to new treatments for dementia within a decade. Scientists will screen compounds that have already been licensed for other conditions, to see if they have any effect on the causes of Alzheimer’s disease.

Jeremy Hughes, chief executive of Alzheimer’s Society, said not enough clinical trials for dementia were taking place in the UK. “We need £4,000 every day for the next 10 years for the first phase of this groundbreaking initiative, and we are asking all those concerned with dementia to help us raise this. Together, we can transform hundreds of thousands of lives.”

If you are going to be a healthcare provider, you must ask the proper questions to your patient…in order to get to the root of the problem. Remember the patient is seeking you out to resolve certain health problems that affect their daily living. We must leave no stone uncovered…ask more questions…spend more time with your patients…

Many soon to be doctors,physical therapists,nurses, and other health professionals need to learn how to read and write a SOAP note. The video above gives a short simple explanation of how to do one. I hope many of my students will find it as a good review.

Superbugs will inherit the Earth…thats exactly where we are headed. Doctors have been over prescripting antibiotics for years…and the bacteria are now becoming resistant to the medication that used to so effective in eliminating them. Health professionals are concern that we may be on borrowed time before a serious pandemic holds this world hostage. We need to investigate new options in controling the continued proliferation of superbugs…science needs to find an answer.

In what has surely become the most ritualised medical practice since the Hippocratic Oath, the World Health Organization took to the stage again today to warn that the misuse of antibiotics was threatening to render one of our most potent medicines useless. This comes a decade after an identical appeal from the organisation warned of a global crisis in the making.

Health experts have been ringing the alarm over antimicrobial resistance for so long that it seems to have become part of our collective background noise, like the endless rasp of waves on the shore. And like stupid tourists, we sleep in the sun while the tide comes in.

It might surprise you to learn that resistance to antibiotics was identified even before Fleming’s wonder drug hit the shelves. The first clinical application of penicillin came in the early 1940s, but the discovery of beta-lactamase – a bacterial enzyme capable of destroying penicillin – preceded that revolution by a few years. The microbes were always one step ahead. As early as 1960, it was clear that overuse of antibiotics was driving the emergence of resistant species.

We also knew how to combat the problem: restricting the use of antimicrobials, ensuring patients completed their courses, containing outbreaks of resistant species. But despite repeated appeals at every level, we couldn’t match the tenacity of microbes. Last year, resistant bacterial infections killed around 25,000 people in Europe alone.

In 2008 the rising waters were finally lapping at our feet. An unusually hardy strain of Klebsiella pneumoniae was isolated from a 59-year-old Swedish patient who had been treated in a New Delhi hospital. The bacterium was found to be indifferent to even our most powerful antibiotics. To make matters worse, the genes that gave it this superpower were found on a small ring of DNA that is easily traded between different species of bacteria.

New Delhi metallo-beta-lactamase (NDM-1) has since turned up in more than 16 countries across the world, including Britain. A study published in Lancet Infectious Diseases today shows the resistance factor has spread to 14 different species of bacteria, including pathogenic varieties responsible for dysentery and cholera. Most bacteria holding the NDM-1 plasmid are resistant to all but a couple of our most clumsy, brutal antibiotics. One strain is immune to all of them.

These are not hollow words. Beyond antibiotics, we have few options left on the table. New antibiotics take around 10-20 years to develop, and there are few in the pipeline. Vaccines are the most obvious alternative, but vaccination programmes are challenging to run even in the most industrialised societies.

Scientists have been training viruses to chase down bacterial cells like packs of hunting dogs for the better part of a century, but Georgia is the only country in the world where such phage therapy is licensed. More exotically, an experimental procedure using a jet of ionised argon gas shows promise, although it can only treat external infections.

After a torrent of dramatic headlines, interest in NDM-1 fell away. After all, in a world well-stocked with superbugs – MRSA, MDRTB, C diff – what was another acronym? The media tend to train their spotlight on highly pathogenic diseases – those that kill in no time flat – at the expense of untreatable diseases, which are far less dramatic. The trouble with superbugs like NDM-1 is that once they gain a foothold in hospitals, even minor surgerical procedures are burdened with a much higher risk of serious postoperative complications.

Last year, the chairman of the Board for the Canadian Committee on Antibiotic Resistance, Professor John Conly, spoke out on the issue. I asked him why NDM-1 had elicited such little concern. “None of us have the answers as to why the issue of antimicrobial resistance does not capture more meaningful attention by governments and governmental agencies,” he wrote. “The problem is that it is somewhat akin to climate change and so slow and insidious that people, and notably our politicians, are lulled asleep.”

Although previous campaigns in France and the USA have achieved substantial reductions in the prescription of antibiotics, their uncontrolled use in other countries has undermined those successes – microbes do not respect national borders. As such, the failure of governments to control drug resistance has often been labelled a “tragedy of the commons”.

But there’s a crucial difference. Left to their own devices, forests and fisheries restock themselves. Medicine cabinets don’t. Even if we rein in our appetite for antibiotics, NDM-1 is here to stay. Perhaps that will be enough to prompt the action called for by health practitioners 50 years ago, but it’s hard to shake the feeling that the microbes have us in checkmate.

The above video is a review of the ligaments of the knee. The ligaments discussed are medial collateral,lateral collateral,medial meniscus,lateral meniscus,posterior cruciate,anterior cruciate. The bone structures that make up the knee are tibia,fibula, and femur.

IF VIDEO IS SLOW…PAUSE IT AND ALLOW 30 SECONDS TO UPLOAD AND CLICK PLAY AGAIN

A medical university class on how to conduct a proper patient interview. In this segment the doctor introduces some useful clinical documents that can facilitate patient care. Stay tune for other videos on this similar topic.

I really enjoyed reading this article and emphasizes that old saying “you are what you eat”. Nutrition plays such an inportant role in how long we eventually live and determines our resistance to disease. A mother’s nutrition has an even more important decision on how your health will reveal itself. But I am also a believer that we can overcome poor nutrition despite our history. There are more cases of poor nutrition during pregnancies around this world that we can count. Life always finds a way to overcome all obstacles and if we seek good nutrition even afterwards, we can eliminate deficiencies and further disadvantages that were brought about by poor eating habits.

Women who have a poor diet during pregnancy may have children who are more susceptible to age-related diseases than those who have a healthier diet, scientists say.

The warning comes after research found that rats that had poor nutrition during pregnancy gave birth to young with a high risk of type 2 diabetes, an illness that typically strikes in middle age.

Researchers at Cambridge University traced back the effect to subtle genetic changes that normally accumulate with age. Similar changes are likely to occur in humans.

The work is believed to be the first evidence that poor maternal diet during pregnancy can make people more vulnerable to the effects of ageing.

Type 2 diabetes affects the way the body produces and responds to insulin, a hormone made by beta cells in the pancreas. The disease is mostly diagnosed in the over-40s, but is becoming more common in younger people.

Scientists led by Susan Ozanne at the Institute of Metabolic Science in Cambridge found that a poor maternal diet led to so-called epigenetic changes that reduced the activity of a gene called Hnf4a in a mother’s young. The gene governs how many insulin-producing cells grow in the pancreas and the organ’s ability to respond to high levels of glucose in the blood.

“It’s well known that maternal diet and growth of the fetus in the womb impact on the risk of developing type 2 diabetes and cardiovascular disease in later life, but we haven’t known the mechanism before,” Ozanne said.

In the study, rats were fed on either a nutritionally poor diet of 8% protein, or a normal diet containing 20% protein. Both had the same number of calories.

While genetic mutations can have an immediate effect on a person’s health, epigenetic changes are more subtle and can take decades to cause problems.

“It is remarkable that maternal diet can mark our genes so they remember events in very early life,” said Miguel Constancia, a co-author on the paper.

People born to mothers who ate badly during their pregnancy are not destined to develop the illness, Ozanne said. “Diabetes is a very multifactorial disease and poor nutrition and growth in early life is just one risk factor.

“It doesn’t mean you will definitely get type 2 diabetes, it just increases your risk. If you have that risk, it is probably a good idea to ensure your adult lifestyle is going to reduce other risks, for example by having a very active life, eating a good diet and not smoking,” Ozanne said.

This is a Korean student of mine from the oriental medical/nursing department learning to do a patient examination and history in English. She also needed to complete a SOAP note that is required of all doctors to properly diagnose and manage treatment. She did an excellent job!

1. What brings you in today?

2. Can you tell me where it hurts?

3. When did this first start?

4. Has this ever happen before?

5. How did you get hurt?

6. Are there any other symptoms?

7. Can I examine you?

8. Does it hurt here?

9. Can you rate this pain on a scale from 1 to 10 …10 being the most pain imaginable..

10. Are you on any other medications?

11. Do you have any allergies?

12. Are you allergic to any medications?

13. Lets take some x-rays.

14. I will prescribe some pills (medication) for 3 days.

15. Go home and put cold packs to the area ..3 times/a day/20 minutes for 3 days

16. If you are still experiencing pain after 3 days..please return to the clinic.

Hey I can use a thinking cap…this idea goes back a long way …I remember watching “Lost in Space”….didn’t the evil Doctor Smith had use of one on the show? This research could have some further applications in the near future. Got an idea to talk about? Send it to YepodShoutout@gmail.com

Scientists have made people better problem solvers by applying tiny electric currents to their brains.

A gentle zapping appeared to free people from taking narrow approaches to cognitive tasks, by stimulating some regions of the brain and dampening down the activity in others.

Scientists at the University of Sydney who led the research said the work was a stepping stone towards a “dream device” that could let people see the world afresh.

The technique, called transcranial direct current stimulation (tDCS), sends apparently harmless, minuscule currents across the brain through conductive pads placed on the skull.

In the first phase of the study, 60 healthy volunteers aged 18 to 38 were set a series of problems that used matchsticks to spell out false mathematical statements with roman numerals, such as III=IX-I. To solve this particular puzzle, the matches must be rearranged as follows: III=IV-I.

The participants worked on 27 similar problems to get their brains in the habit of solving problems in a particular way. Afterwards, each volunteer was stimulated with a 1.6 milliamp current, or assigned to a control group that received the same procedure with the electricity switched off.

Five minutes later, the volunteers tackled two more sets of matchstick puzzles that required slightly different approaches, for example VI = VI + VI. In this case, the problem is solved by modifying the operator instead of the number, to give: VI = VI = VI.

The researchers found that volunteers who had electrical stimulation to their anterior temporal lobes were three times more likely to acquire the fresh insight needed to complete puzzles than the control group. The study appears in the journal, Plos One.

“Our findings demonstrate the possibility that we can modulate cognitive tradeoffs to our advantage in certain situations,” Allan Snyder, director of the Centre for the Mind at the University of Sydney, told the Guardian. “They are proof of concept for the “dream” device, one that allows us to temporarily see the world anew, freeing us from entrenched mindsets.”

The benefits were only seen when tDCS dampened down activity in the left anterior temporal lobe, which is associated with conceptual processing, labels and categorising, and stimulated activity in the right anterior temporal lobe, linked to insight and novel meaning.

“By artificially inducing a less filtered view of the world, we believe we can temporarily allow a less assumption-driven cognitive style, one that is crucial for creative leaps,” Snyder said.

Last year, Roi Cohen Kadosh, a researcher at Oxford University, reported tDCS experiments that improved people’s ability to learn mathematics. He said Snyder’s work was “exciting evidence that the technique can also be used to enhance innovative thinking, or “thinking outside the box”.”

“As it becomes more fashionable to use some types of drugs for cognitive enhancement, this method seems to be a good, safe, and attractive alternative,” Cohen Kadosh said.

Wow ..dogs being trained to sniff out illnesses or cancers in people? Well yes…it makes sense..dogs have a unique sense of smell as with many other animals. Would be great to have your own dog trained to be able to smell your body and alert you if there was a problem…I see a market here…hey I would pay to get my very own” illness sniffing dog” to warn me if a problem with my health develops…

Dogs can be trained to sniff out bowel cancer, even when the disease is in its early stages, researchers in Japan claim.

In a series of experiments that involved sniffing the breath or stool samples of patients, a specially-trained labrador retriever proved nearly as good at identifying those with cancer as a conventional colonoscopy examination.

The team, led by Hideto Sonoda at Fukuoka dental college hospital, said some dogs have such a keen sense of smell that they can detect minute traces of chemicals that appear to circulate in the bodies of people who have cancer.

The finding builds on previous experiments in which researchers used dogs to sniff out cancers in the skin, lungs, bladder and ovaries.

Writing in the journal Gut, the researchers describe how the eight-year-old dog was trained to distinguish between the smell of a patient with colorectal cancer and a healthy volunteer, using samples of their breath alone.

In later tests, the dog correctly identified 33 of 36 people with bowel cancer after sniffing their breath, and 37 of 38 cancer cases after sniffing a stool obtained from the patient.

The findings are expected to help scientists identify aromatic chemicals in the body that betray the early signs of bowel cancer and can be detected by medical sensors.

An effective test for bowel cancer, called the faecal occult blood test, picks up hidden blood in a stool sample, but is only able to detect early stage disease in one in 10 cases, the researchers said.

“It would be extremely difficult to use dogs as part of routine testing for cancer, and that’s why further research in this area is concentrating on finding out more about the molecules given out by tumours, to see if they could be detected in other ways.”